Search PubMed⌕ Search

Biomedical subjects

N Yuki

Publications and source records attributed to N Yuki.

At least 109 records · Page 6Linked to original sources
PubMed1999

Survival of a probiotic, Lactobacillus casei strain Shirota, in the gastrointestinal tract: selective isolation from faeces and identification using monoclonal antibodies.

Lactobacillus casei strain Shirota (LCS) is a probiotic bacterium used in the production of fermented milk products and lactic acid bacteria preparations. To investigate the survival of LCS in the gastrointestinal tract, we have developed a selective medium and specific monoclonal antibodies to isolate and identify this strain. Selective LLV agar medium was prepared by modifying LBS medium, a selective medium for lactobacilli, through the replacement of glucose with lactitol as a carbon source and vancomycin as a selective antibiotic. Culture in LLV agar medium followed by ELISA using monoclonal antibodies specific for LCS was able to detect the organism in faeces. Using this method, we studied the faecal recovery of LCS in individuals who drank 125 ml of fermented milk which contained 10(10) live LCS for 3 days. The mean recovery was about 10(7) live bacteria per gram of faeces, indicating that LCS survived transit through the gastrointestinal tract after ingestion of the fermented milk.

Adult↗
PubMed1999

Antibodies to GD3, GT3, and O-acetylated species in Guillain-Barré and Fisher's syndromes: their association with cranial nerve dysfunction.

We examined serum antibodies to the four fetal antigens GD3, O-acetyl GD3, GT3, and O-acetyl GT3 ganglioside in patients with Guillain-Barré syndrome (GBS) or its variant Fisher's syndrome (FS). The patients with FS more often had significant IgG antibodies against GD3, GT3, and O-acetyl GT3 than did the healthy controls. Furthermore, anti-GD3 and anti-GT3 IgG antibodies were more often significantly present in the patients with FS than in those with GBS. IgG antibody to GD3, GT3, and O-acetyl GT3 had a significant association with the presence of ophthalmoparesis. These antibodies, however, cross-reacted with GQ1b and we detected no antibodies which specifically reacted with fetal gangliosides. In addition, oculomotor involvement was more closely related to IgG antibodies to GQ1b than to those to fetal gangliosides. No evidence was obtained that the serum antibodies to these fetal gangliosides are associated with specific neurologic signs of cranial nerves.

Cranial Nerve Diseases↗
PubMed1999

Are Campylobacter curvus and Campylobacter upsaliensis antecedent infectious agents in Guillain-Barré and Fisher's syndromes?

Campylobacter curvus and Campylobacter upsaliensis were isolated from stools of patients with Guillain-Barré (GBS) or Fisher's (FS) syndromes. Whether these microorganisms are pathogens of antecedent diarrhea in GBS and FS is not clear, therefore, we made a serological examination. There were no differences in antibody titer to these organisms among the patients with GBS, FS, and the controls. Some patients had elevated antibodies to the bacteria, but most also had serological evidence of C. jejuni infection. Moreover, the patients from whom C. curvus had been isolated did not have antibodies to the bacterium, indicative that they were healthy carriers of C. curvus or that the isolates were the product of contamination. We conclude that neither C. curvus nor C. upsaliensis is the major agent of antecedent diarrhea in GBS and FS.

Antibodies, Bacterial↗
PubMed1999

The 301 to 314 amino acid residue of beta-tubulin is not a target epitope for serum IgM antibodies in chronic inflammatory demyelinating polyneuropathy.

Connolly et al. [Neurology 48 (1997) 243] reported that IgM M-proteins from three patients selectively binds to an epitope on beta-tubulin that consists of amino acids 301 to 314. We therefore investigated whether these 14 amino acid residues beta301-314 are the target epitope for serum IgMs in sera from 67 patients with chronic inflammatory demyelinating polyneuropathy (CIDP), 50 with Guillain-Barré syndrome, 50 with motor neuron diseases, and 50 normal controls. IgM anti-beta301-314 antibodies were not restricted to nor were selectively associated with CIDP. We conclude that beta301-314 is not a target epitope for serum IgMs in CIDP.

Autoantibodies↗
PubMed1999

Clinical implications of coinfection with a novel DNA virus (TTV) in hepatitis C virus carriers on maintenance hemodialysis.

A novel hepatitis-associated DNA virus, designated as transfusion-transmitted virus (TTV), was identified recently. We investigated the frequency of TTV viremia in hepatitis C virus (HCV) carriers on maintenance hemodialysis to determine whether TTV coinfection has any clinical relevance. The subjects were 50 hemodialysis patients who had been followed over 4 years after diagnosis of HCV infection. Stored serum samples derived from each patient every 12th month after enrollment were subjected to polymerase chain reaction to amplify TTV DNA and HCV RNA. At enrollment, TTV viremia was detected in 24 (48%) HCV-positive patients irrespective of the number of previous blood transfusions and the duration of hemodialysis. The presence of TTV viremia had no relation to serum alanine aminotransferase (ALT) levels, HCV viremic levels or HCV genotypes. After enrollment, HCV infection persisted in all patients over the 4-year follow-up period, whereas spontaneous resolution of TTV infection was observed in 7 (29%) of the 24 TTV viremic cases (annual rate 7.3%, 95% confidence interval [CI] 0.8-25.5%). Evidence for TTV infection was found in 4 (15%) of the 26 TTV nonviremic patients (annual incidence 3.9%, 95% CI 0.1-19. 6%). The relationship between the ALT profile and TTV infection during follow up was not evident. Active TTV coinfection occurs frequently in HCV carriers undergoing hemodialysis but exerts no biochemical or virological influence on the underlying hepatitis C. Lack of disease association and the frequent spontaneous resolution of infection suggest that the clinical significance of TTV infection remains unclear.

Adult↗
PubMed1999

Axonal involvement at the common entrapment sites in Guillain-Barré syndrome with IgG anti-GM1 antibody.

If anti-GM1 antibody plays a role in the axonal damage in Guillain-Barré syndrome, the common entrapment sites may be preferentially involved with evidence of axonal dysfunction. To assess this hypothesis, we studied nerve conduction across the cubital tunnel in 44 patients. Abnormal amplitude reduction of compound muscle action potentials (CMAPs) was found in 45% of 20 immunoglobulin G (IgG) anti-GM1-positive and in 29% of 24 anti-GM1-negative patients. The time course and sequel were distinct between the two groups. In the former group, the amplitude reduction was prominent in weeks 1 to 2 and was followed by a decrease in distal CMAPs (axonal degeneration) or an increase in proximal CMAPs (resolution of conduction block). In contrast, anti-GM1-negative patients showed slower resolution with temporal dispersion. In anti-GM1-positive cases, amplitude reduction at the common entrapment site is frequent and may reflect wallerian degeneration or physiological conduction block at the nodes of Ranvier, both suggesting axonal involvement.

Action Potentials↗
PubMed1999

Special sensory ataxia in Miller Fisher syndrome detected by postural body sway analysis.

To investigate whether ataxia in Miller Fisher syndrome (MFS) is caused by loss of proprioception or cerebellar dysfunction, we studied the power spectrum peak of the body sway frequency in 10 MFS patients, and compared the results with those of patients with cerebellar or sensory ataxia. The cerebellar patients had a peak at 2.4 Hz, whereas sensory ataxia patients had a 1-Hz peak. Nine of the MFS patients had a distinct 1-Hz peak. Clinical sensory loss or abnormal sensory nerve potentials were present in only 3 patients, whereas soleus H-reflexes were absent in all the MFS patients. MFS patients have dysfunction of the proprioceptive afferent system, and the special sensory ataxia may be caused by the selective involvement of muscle spindle afferents.

Adult↗
PubMed1999

Antiganglioside antibody in patients with Guillain-Barré syndrome who show bulbar palsy as an initial symptom.

OBJECTIVES: To identify valuable antiganglioside antibodies that support the diagnosis of Guillain-Barré syndrome (GBS) and its variants in patients showing bulbar palsy as an initial symptom. METHODS: Medical records of 602 patients with GBS or its variants were reviewed. Fifteen patients had bulbar palsy as an initial symptom. Serum antibodies against GM1, GM1b, GD1a, GalNAc-GD1a, GT1a, and GQ1b were examined in 13 of them. RESULTS: Serum antiganglioside antibodies were positive in 11 (85%) patients. IgG anti-GT1a (n=8; 62%) and anti-GM1b (n=7; 54%) antibodies were often present, whereas all the patients had low or no anti-GM1 antibody activity. High anti-GD1a and anti-GQ1b IgG antibody titres were also present in some patients, but most had higher IgG antibody titres to GM1b or GT1a. All five patients with high IgG antibody titre to GM1b or GT1a only had had antecedent diarrhoea. Some patients with pharyngeal-cervical-brachial weakness (PCB) had IgG antibody to GT1a which did not cross react with GQ1b. Other patients with PCB had antibody to GT1a which cross reacted with GQ1b or antibody to GM1b, but anti-GM1b and anti-GT1a antibodies were not associated with the presence of bulbar palsy. All the patients who had no IgG antiganglioside antibodies recovered completely. CONCLUSIONS: Measurement of serum IgG anti-GT1a and anti-GM1b antibodies gives helpful support for the diagnosis of GBS and its variants when there is early involvement of the oropharyngeal function independently of other neurological findings which appear as the illness progresses.

Adolescent↗
PubMed1999

Hyperreflexia in Guillain-Barré syndrome: relation with acute motor axonal neuropathy and anti-GM1 antibody.

OBJECTIVES: To investigate the incidence of hyperreflexia in patients with Guillain-Barré syndrome (GBS), and its relation with electrodiagnosis of acute motor axonal neuropathy (AMAN), antiganglioside GM1 antibody, and Campylobacter jejuni infection. It was reported that patients with AMAN in northern China often had hyperreflexia in the recovery phase. METHODS: In 54 consecutive Japanese patients with GBS, sequential findings of tendon reflexes were reviewed. By electrodiagnostic criteria, patients were classified as having AMAN or acute inflammatory demyelinating polyneuropathy (AIDP). Anti-GM1 and anti-C jejuni antibodies were measured by enzyme linked immunosorbent assays. RESULTS: Seven (13%) patients developed hyperreflexia with the spread of the myotatic reflex to other segments in the early recovery phase, one of whom already had hyperreflexia in the acute progressive phase. Of the seven patients, six had AMAN and all seven had anti-GM1 antibodies, whereas only two had anti-C jejuni antibodies. Hyperreflexia was more often found in patients with AMAN than AIDP (6/23 v 1/18, p=0. 002), and in patients with anti-GM1 antibodies than without them (7/26 v 0/28, p=0.01). Hyperreflexic patients had milder peak disabilities than patients without hyperreflexia (p=0.03). Increased motor neuron excitability in the hyperreflexic patients was supported by increased soleus H-reflex amplitudes and the appearance of H-reflexes in the small hand or foot muscles. CONCLUSIONS: Hyperreflexia often occurs in patients with GBS especially with AMAN, anti-GM1 antibodies, and milder disease. Increased motor neuron excitability further characterises the subgroup of patients with GBS with AMAN and anti-GM1 antibodies.

Acute Disease↗
PubMed1999

Bilateral ballism in a patient with overlapping Fisher's and Guillain-Barré syndromes.

A 29 year old woman developed diplopia and ataxic gait. Neurological examination showed total ophthalmoplegia, cerebellar ataxia, and areflexia. Moreover, there was muscle weakness in all four limbs. An overlap of Fisher's and Guillain-Barré syndromes was dignosed. On day 5 she suddenly developed involuntary flinging movements that affected the face and four limbs. Surface EMG showed 1.5-2 Hz rhythmic grouping discharges. The involuntary movements were considered ballism. This is the first report of a patient with Guillain-Barré syndrome and a related disorder who showed ballism.

Adult↗
PubMed1999

IgG anti-GQ1b positive acute ataxia without ophthalmoplegia.

IgG anti-GQ1b antibody was present in a patient with acute ataxia and areflexia without ophthalmoplegia or elementary sensory loss. Sensory nerve conduction studies and somatosensory evoked potentials were normal, but postural body sway analysis showed dysfunction of the proprioceptive afferent system. The clinical presentation and laboratory results for this patient resemble those of Miller Fisher syndrome, except for the lack of ophthalmoplegia. This case may represent part of an IgG anti-GQ1b syndrome.

Acute Disease↗
PubMed1999

[Campylobacter jejuni enteritis and Guillain-Barré syndrome].

Guillain-Barré syndrome (GBS) is the most common cause of acute neuromuscular paralysis. Sera from patients with GBS following Campylobacter jejuni infection frequently have autoantibody to GM 1 ganglioside in the acute phase of the illness. We revealed that the lipopolysaccharide (LPS) of C. jejuni that was isolated from a GBS patient has the oligosaccharide structure [Gal beta 1-3 GalNAc beta 1-4 (NeuAc alpha 2-3) Gal beta 1-], which is identical to the terminal tetrasaccharide of GM 1 ganglioside. (1) Infection by C. jejuni that bears the GM 1-like lipopolysaccharide associated with the serotypic determinant of PEN 19 induces high production of IgG 1 and IgG 3 anti-GM 1 antibodies with help of T cells. (2) IgG anti-GM 1 antibody binds to motor nerve terminal axons, inhibits motoneuron excitability, and produces the development of GBS.

Animals↗